43/100
Amyloid-beta (Aβ) oligomers are thought to trigger Alzheimer's disease pathophysiology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
43/100
Expression of long-lasting synaptic plasticity and long-term memory requires protein synthesis, which can be repressed by phosphorylation of eukaryotic initiation factor 2 α-subunit (eIF2α). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic abnormalities are a cardinal feature of Alzheimer's disease (AD) that are known to arise as the disease progresses. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We show that a natural behavior, exploration of a novel environment, causes DNA double-strand breaks (DSBs) in neurons of young adult wild-type mice. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress is a component of many diseases, including atherosclerosis, chronic obstructive pulmonary disease, Alzheimer disease and cancer. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ferroptosis is an iron-dependent cell death, which is different from apoptosis, necrosis, autophagy, and other forms of cell death. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress has been implicated in the pathogenesis of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In AD, the presence of a lifetime history of depression corresponds to increases in AD-related neuropathological changes within the hippocampus. 4 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder molecularly characterized by the formation of amyloid β (Aβ) plaques and type 2 microtubule-associated protein (Tau) abnormalities. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, AD, is the most common form of dementia. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Neurological degeneration after neuroinflammation, such as that resulting from Alzheimer's disease (AD), stroke, multiple sclerosis (MS), and post-traumatic brain injury (TBI), is typically associated with high mortality and morbidity and with permanent cognitive dysfunction, which places a heavy economic burden on families and society. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease with no cure. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We describe a hitherto unknown feature for 27 small drug-like molecules, namely functional inhibition of acid sphingomyelinase (ASM). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Perivascular spaces (PVS) are compartments surrounding cerebral blood vessels that become visible on MRI when enlarged. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The evident genetic, pathological, and clinical heterogeneity of Alzheimer's disease (AD) poses challenges for traditional drug development. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial dysfunction is an established hallmark of aging and neurodegenerative disorders such as Down syndrome (DS) and Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Overexpression of the amyloid precursor protein (APP) gene on chromosome 21 in Down syndrome (DS) has been linked to increased brain amyloid levels and early-onset Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques contain many proteins in addition to beta amyloid (Aβ). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Because even the very mildly demented brains showed substantial pathological change, emphasis was placed on examining the nondemented cases for the earliest changes that could be associated with Alzheimer's disease. 2 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Neuronal loss is the central issue in Alzheimer's disease (AD), yet no treatment developed so far can halt AD-associated neurodegeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The escalating prevalence of Alzheimer's disease (AD) highlights the urgent need to develop reliable biomarkers for early diagnosis and intervention. 2 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Phospho-tau protein p-tau181 is a cerebrospinal fluid biomarker for Alzheimer's disease (AD), while p-tau217 is the most sensitive plasma biomarker for cerebral amyloid β (Aβ) load prior to tau pathology in preclinical AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The levels of p-tau217 and p-tau231 in cerebrospinal fluid (CSF) are associated with early amyloid beta (Aß) changes in the brain, while the CSF levels of p-tau205 are foremost related to tau pathology in the later stages of the disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder and represents a major public health challenge. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 7,799 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Tau proteins in blood as biomarkers of Alzheimer's disease and other proteinopathies
- A new era in neuropharmacology: assessing the efficacy and safety of novel anti-amyloid and non-amyloid drug targets for Alzheimer's disease
- Alpha-synuclein co-pathology in a real-world early Alzheimer's disease cohort
- Accelerated in vitro fibril formation by a mutant alpha-synuclein linked to early-onset Parkinson disease
- Glial dysfunction in the pathogenesis of α-synucleinopathies: emerging concepts
- Sensorineural hearing loss may lead to dementia-related pathological changes in hippocampal neurons
- Spatial reversal learning defect coincides with hypersynchronous telencephalic BOLD functional connectivity in APP NL-F/NL-F knock-in mice
- Combined neuropathological pathways account for age-related risk of dementia
- Microbiome Alterations and Alzheimer's Disease: Modeling Strategies with Transgenic Mice
- Pathways of cellular proteostasis in aging and disease
Where “Free full text” comes from
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
How the 0–100 score works — and why some entries are capped
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,980 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,038 records (3.6% of the library) are not peer-reviewed — 966 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →